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Nursing > Pharm Exam II > Flashcards

Pharm Exam II Flashcards

1
Q

Hypertension

A

Prevalent and common chronic disorder that affects 50-60 million adults. Can be very dangerous. If left untreated, you can have a greater risk for CHF, cardiac infarction, cerebral infarction. Kidney failure due to high blood pressure running through the sensitive tissue.

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2
Q

Angiogram

A

put dye through someone’s bloodvessels to see if there is blockage in the heart

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3
Q

Function of Cardiac Cycle

A

Bring oxygen to the myocardium and tissues

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4
Q

Pulmonary Artery

A

only artery that carries deoxygenated blood.

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5
Q

2 phases of Cardiac Cycle

A

Systole and Diastole

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6
Q

Systole

A

contraction of the ventricles of the heart that occurs between the first and second heart sounds of the cardiac cycle

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7
Q

Diastole

A

the part of the cardiac cycle during which the heart refills with blood after the emptying done during systole. Resting state

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8
Q

Stroke Volume

A

amount of blood ejected from the left ventricle with each contraction

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9
Q

Preload

A

end-diastolic volume. Amount of blood left in the left ventricle

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10
Q

Afterload

A

resistance to left ventricular ejection: the work the heart must overcome to eject blood.

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11
Q

Contractility

A

Ability of the heart muscle to contract

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12
Q

Cardiac Output

A

amount of blood pumped by the heart each minute

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13
Q

Cardiac Output Equation

A

Heart Rate x Stroke Volume

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14
Q

Cardiac Conduction Pathway

A

SA node:AV node:BUndle of HIS:Right+Left Bundle Branches:Purkinje Fibers

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15
Q

SA node

A

pacemaker of the heart

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16
Q

Atrioventricular Node

A

Receives the message from the SA node. Has the ability to slow so that the ventricles fill properly. This is the filter

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17
Q

Purkinje Fibers

A

Causes the contraction or squeeze of the ventricles

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18
Q

Cardiac Blood Flow

A

Venous Deoxygenated return to heart
arterial oxygenated outflow to the body
Venous pressure system is lower so it needs valves

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19
Q

Pulse Pressure

A

This number represents the filling pressure of the arteries

Systolic blood pressure minus diastolic blood pressure.

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20
Q

Vasomotor Center

A

Made up of Baroreceptors and Chemoreceptors

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21
Q

Chemoreceptors

A

respond to oxygen, carbon dioxide, and pH changes, increases or decreases

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22
Q

Baroreceptors:

A

respond to increase of decrease in pressure or stretch

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23
Q

Anger or stress effect on BP

A

elevates your blood pressure

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24
Q

Depression or lethargy

A

deplete blood pressure

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25
Q

Antidiuretic Hormone (ADH)

A

released to increase blood pressure. This will keep the fluid volume in your body. It is going to NOT produce this when you are HTN because it wants you to get rid of blood volume

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26
Q

Renin-angiotension-aldosterone system (RAAS)

A

blood pressure regulation by modulating blood volume, sodium reabsorption, potassium secretion, water reabsorption, and vascular tone

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27
Q

Peripheral Resistance/Diameter of arterioles

A

how much pressure is in the arterials/lack of pressure in the venous system. This is emphasized by sympathetic nervous system activity. Activation of SNS. Has effect on BP

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28
Q

Viscosity

A

increase in blood viscosity is typically related to dehydration and will raise the blood pressure.

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29
Q

Lack of O2 effect on BP

A

increase because the body thinks that it is time to speed up for proper perfusion

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30
Q

Cellular metabolism by-product accumulation effect on BP

A

(CO2/lactic acid). Occurs when people are septic

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31
Q

Histamine

A

release dilates blood vessels/lowers BP

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32
Q

Bradykinin

A

potent peptide causing vasodilation/lowers BP

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33
Q

Prostaglandin

A

includes both vasodilators and vasoconstrictors

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34
Q

Arterial blood Pressure:

A

force exerted on arterial walls by blood flow. This is most affected by Systolic BP and Diastolic BP

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35
Q

Frank Starling Law

A

The more volume of blood in the heart during diastole, the more forceful the cardiac contraction, the more blood the ventricle will pump.

Exception: cardiomyopraphy

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36
Q

cardiomyopraphy

A

the muscles of the heart get stretched out

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37
Q

When the body’s blood pressure increases, two things might happen:

A
  1. Compensatory action by the cardiovascular system might occur which will cause vasodilation, decreased stroke volume, decreased heart rate (which will in turn decrease the cardiac output). All of these things will lower the blood pressure
  2. Compensatory action by the kidney’s: increased urine output will decrease the blood urine which will decrease the BP
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38
Q

Hypotension

A

Systolic less than 90

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39
Q

Response to Hypotension

A

SNS is stimulated.

  • Adrenal medulla secretes epinephrine and norepinephrine
    -Angiotensin II and aldosterone are formed
    -Kidney’s retain fluid and blood pressure is increased
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40
Q

Response to Hypertension:

A

Increases renal secretion (increases urine output), fluid loss, less circulating volume, decrease in cardiac output, decrease in arterial blood pressure

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41
Q

Definition HTN

A

persistently high blood pressure (increase force in arteries) that results from abnormalities in regulatory mechanism.

Systolic pressure greater than 140mmHg
Diastolic Pressure greater than 90mmHg

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42
Q

PreHTN

A

S=120-139|D=80-90

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43
Q

Stage 1 HTN

A

130-139

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44
Q

Stage 2 HTN

A

140+

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45
Q

Primary HTN

A

90%-95% of cases: complex physiological condition where the cause is unknown.

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46
Q

Secondary HTN

A

may result from renal artery stenosis, endocrine, or CNS disorders from medications. Results from an identifiable cause. We know why they have it.

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47
Q

Effects of BP

A

MI (tires out the heart), CHF, stroke, renal disease, retinal damage

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48
Q

myocardial hypertrophy

A

muscle works hard, but it doesnt get bigger in to out. It gets bigger out to in. The walls start to thicken and it reduces the size of the ventricles which reduces perfusion

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49
Q

ADH: (Antidiuretic Hormone):

A

released in response to an increase in blood osmolality (blood gets thicker in a dehydrated state)
Promotes reabsorption of water by the kidneys to try to get the thicker blood to be thinner.
Decreases the urine output
INcrease in circulating blood volume which will in turn increase the Na+ and water in the body
Loss of K+ in urine
Potent vasoconstrictor
Synthetic vasopressin admin to treat DI and hypotensive crisis

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50
Q

Renin-Angiotensinogen-Aldosterone System

A

Liver constantly produces angiotensinogen in the plasma
Renin is produced in response to low BP which reacts with angiotensinogen to make angiotensin I
Angiotensin converting enzyme takes the angiotensin 1 and makes it angiotensin 2 which produces aldosterone (rom adrenal cortex)
This causes reabsorption of Na+ and H2O

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51
Q

White coat syndrome

A

afraid to come to the doctor’s office and their blood pressure goes up.

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52
Q

Non-Pharmacological Agents to help with BP:

A

Stress management
Limit ETOH (alcohol) (male 2 or less a day. Women 1 to less a day)
REduce sodium
Reduce fat and cholesterol
Increase fruit and vegetables
Increase aerobic physical activities
Discontinue tobacco products
Maintain optimum weight

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53
Q

Angiotensin Converting Enzyme Inhibitors: ACE inhibitors

A

Inhibit the conversion of angiotensin I to angiotensin II
-Ex. CaptoPRIL, enalaPRIL, lisinoPRIL, remiPRIL

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54
Q

ACE I side Effects:

A

ACE cough (ticky cough)
Angioedema (swelling around oral cavity that is a 911)
Hyperkalemia. Avoid K+ supplements, K sparing diuretics, or foods high in K+, or salt substitutes
Orthostatic hypotension
Peptic Ulcers, gastric irritation
Acute renal failure (kidneys regulate K+)
HA/Dizzy

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55
Q

When to take ACE

A

Take 1 hour before or 2 hours after a meal (lisinopril can be taken with food)

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56
Q

Black Box ACE

A

causes injury and death to fetus

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57
Q

Angiotensin II Receptor Blockers (ARBs):

A

Selectively bind to angiotensin II receptors in vascular smooth muscle and adrenal cortex.

Insurance wont pay for these ones upon first visit

Ex. Losartan, Valsartan, olmesartan

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58
Q

ARB side effects:

A

Orthostatic Hypotension
HA, dizziness, diarrhea
Dry Mouth
angioedema
Acute renal failure: watch BUN, Creatinine, and GFR
Hyperkalemia: blocking the angiotensin II in the cascade

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59
Q

ARB Dose Dependent:

A

once daily for HTN treatment/Twice daily for CHF monitor K+

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60
Q

Black Box for all ARBS

A

pregnancy: known to cause injury or death to the fetus

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61
Q

Calcium Channel Blockers:

A

Treatment for HTN. Inhibit the movement of Ca+ ions across the membranes of myocardial and arterial muscle cells. Decrease in HR and causes vasodilation of the peripheral vasculature

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62
Q

Medication that are Calcium Channel Blockers

A

amlodipine, diltiazem, verapamil, nicardipine, nifedipine

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63
Q

Ca+ blocker side effects

A

Flushed skin, muscle cramps, peripheral edema
HA, dizziness, hypotension
Impotence, sexual dysfunction
Hepatotoxicity (interacts with alcohol)
Angioedema
Contraindications: renal impairment, CHF/heart block, or pregnancy
Interacts with macrolide antibiotics and grapefruit juice

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64
Q

Antiadrenergic Medications

A

Inhibits the SNS=decreases HR, decreases the force of myocardial contraction, cardiac output, and blood pressure

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65
Q

Alpha1 Adrenergic receptor blockers:

A

dilate blood vessels and decrease peripheral vascular resistance (PVR)

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66
Q

Alpha1 Adrenergic receptor blockers Examples

A

doxazosin, prazosin, terazosin

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67
Q

Side Effects of A1 Adrenergic Blockers

A

first dose phenomenon:ortho-hypotn, dizziness, palpitations, syncopal episode (drops so low they pass out)
First does, increase dose (start low go slow)=given at night to prevent SE
Can have increase Na+/fluid retention

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68
Q

Alpha2-receptor agonists:

A

Inhibits norepinephrine, has an antiadrenergic effect, decreases CO, decrease HR, decreases PVR, decreases BP

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69
Q

Examples of Alpha2-receptor agonists:

A

clonidine (strong), methyldopa, guanfacine

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70
Q

Beta Adrenergic Blockers:

A

Decrease HR, force of myocardial contraction, CO and renin release from the kidneys

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71
Q

Beta Adrenergic Blockers Medications

A

atenolol, metoprolol, propranolol

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72
Q

When to use Beta Adrenergic Blockers:

A

First medication for patients under 50 with cardio selective medications. first choice in patients with asthma, PVD, or DM. Make sure you have a selective beta blocker for asthma or COPD patients

bid or hold for HR less than 60bpm

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73
Q

Beta Adrenergic Blockers TX

A

HTN, Dysrhythmias, HF, MI, and narrow angle glaucoma

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74
Q

Side effects of B-Andrenergic Blockers

A

hypotension, bradycardia, dizziness (caution in pt. With liver impairment)

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75
Q

Black Box for all beta adrenergic blockers

A

Don’t stop abruptly. For patients with CAD (coronary artery disease), dose must be titrated down prior to discontinuing. If not, RF rebound angina (chest pain), vent dysrhythmias, MI

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76
Q

Side effect of Beta Blocker

A

This medication can cause erectile dysfunction.

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77
Q

Alpha-Beta Adrenergic Blockers

A

carvedilol, labetalol.
Dual Action in one tablet

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78
Q

Diuretics

A

Reduction of blood volume through urinary excretion of H2O and electrolytes.

Often used as a first line rx in mild-mod HTN

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79
Q

Thiazide + Thiazide-like diuretics

A

block Na+ reabsorption, increase K+ and H2O secretion
Ex. hydrochlorothiazide

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80
Q

Potassium-sparing diuretics

A

spironolactone

excretion of Na+ and retention of K+
K+ sparing diuretic
Use for someone with low K.

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81
Q

K+ Importance

A

response for contractility of the heart

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82
Q

spironolactone

A

Potassium-sparing diuretics

Can increase effects of digoxin, monitor for hyperKalemia in patients also taking ACE/ARB

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83
Q

Loop Diuretics:

A

Inhibit reabsorption of Na+ and Cl- in the loop of Henle.
K+ wasting diuretic
Furosemide: always monitor K+
Can increase digoxin levels, cause hypoKalemia

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84
Q

Furosemide

A

Loop Diuretic. Can increase digoxin levels

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85
Q

Direct Acting Vasodilators

A

Directly relax smooth muscles in the blood vessels=dilation and decreased PVR

hydralazine, nitroprusside (IV only)

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86
Q

Ventricular Tachycardia

A

very rapid contraction of the ventricles. Very dangerous because the ventricles pump so hard that the heart might lead to cardiac arrest.

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87
Q

Asystole

A

straight line on an EKG.

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88
Q

Dysrhythmia/Arrhythmia

A

abnormality in a physiological rhythm; especially in the activity of the brain or heart

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89
Q

contractile tissue

A

Electricity resides in specialized tissues that generate and conduct electrical impulses

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90
Q

Regular intervals with four events

A

stimulation from electrical impulse=transmission to adjacent tissue=contraction of atria, then ventricles=relaxation of atria, then ventricles

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91
Q

Automaticity

A

ability of the heart to generate an electrical impulse

Any part of conduction system can start an impulse

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92
Q

Conductivity

A

ability of cardiac tissue to transmit the electrical impulse.

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93
Q

Why is the SA node the pacemaker

A

It has the fastest rate of automaticity (pacemaker)

Initiation of the impulse is dependent on Na and K ion movement

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94
Q

Absolute refractory period

A

Period of decreased excitability/cells cannot respond to new stimulation

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95
Q

P wave

A

measures the electrical depolarization of the atria

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96
Q

QRS wave

A

has to do with bundle branches and purkinje network

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97
Q

T wave

A

has to do with ventricular repolarization

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98
Q

Dysrhythmia

A

abnormality in cardiac rate or rhythm
Can originate in any part of the conduction system

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99
Q

Automaticity

A

allows cells other than SA node to initiate electrical impulse that reaches the highest level of contraction
SA node failure to slow depolarization
Built in defense mechanism. AV node can take over if SA node is failing

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100
Q

ectopic focus/ectopic beat

A

Impulse origination other than in SA node
Indicates myocardial irritability

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101
Q

Activation of ectopic focus/ectopic beat

A

Hypoxia (low O2 in blood), ischemia (no blood to tissue), hypokalemia (low potassium)

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102
Q

Tachycardia

A

beating faster than normal. Can occur in Ventricles or Atria.

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103
Q

Sinus Tachycardia

A

normal sinus rhythm with faster than 100bpm

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104
Q

Atrial Flutter

A

atria beat regularly, but faster than normal and more often than the ventricles do. Can be a ratio of 4/1

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105
Q

Atrial Fibrillation

A

atria beat irregularly. The SA node is firing so fast that the AV node cannot keep up with the signals. Classic rhythm strip with NOT have a P wave because the SA node is firing really fast

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106
Q

Asystole

A

no beats. Can be treated with medications.

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107
Q

ROSC

A

Return of Systemic Circulation

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108
Q

Heart Block:

A

Signal between atria and ventricles message pathway is interrupted. This is a medical emergency. Can be partial or total

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109
Q

Sinus Bradycardia:

A

heart beat in a normal sinus rhythm, however, it is under 59 bpm

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110
Q

Prior goal of pharmacotherapy

A

suppress dysrhythmias resulted in higher mortality rate among patients receiving antidysrhythmic drug therapy than those who were not

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111
Q

Antidysrhythmic drugs can

A

worsen existing dysrhythmias, may cause new dysrhythmias

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112
Q

Newest goal of therapy

A

prevent, relieve symptoms and prolong survival

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113
Q

Cardioversion

A

nonpharmacologic strategy: stopping the heart with a shock hoping that the heart beat will come back normal

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114
Q

Defibrillation

A

nonpharmacologic strategy: Vtac and Vfib are shockable by defib.

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115
Q

Radiofrequency Catheter Ablation

A

nonpharmacologic strategy: procedure where the doctor uses a cath to send radiofrequency energy to make circular scars around the heart and cells that are causing the dysrhythmias to burn out the areas and stop those cells from firing.

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116
Q

Pacemakers

A

utilized for sinus bradycardia. Or bradyarrhythmias for people whose heart rate goes below 40. This gives the heart a little shock that forces the heart to beat when it senses the dropped heart rate.

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117
Q

Atrial Fibrillation

A

if the ventricles are contracting too much, blood might be stored in the atria and then stored blood might clot. When that portion of blood gets into the ventricles and then they get into the lungs.

***Must be on some type of blood thinner

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118
Q

Sodium Channel Blockers

A

atrial dysrhythmia, Supraventricular Tachycardia (bursts of high rapid heart rates).

MOA depends on the class (IA, IB, IC) the medication is in

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119
Q

Sodium Channel Blockers SE

A

arrhythmias, Bradycardia, hypotension, respiratory Depression, dizziness, syncope, drowsiness, fatigue, confusion, anticholinergic

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120
Q

Sodium Channel Blockers EX

A

quinidine, lidocaine

Concerns: interfere with anticoagulants (which all atrial fib patients are on) and…obviously not good for someone with respiratory issues

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121
Q

Beta Adrenergic Blockers

A

Reduce activation of beta receptors=decrease conduction through SA/A node=decrease automaticity=slow HR

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122
Q

Beta Adrenergic Blockers Effect

A

Decreases cardiac excitability, cardiac workload, and oxygen consumption
Kinda like a slap to the face

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123
Q

Beta Adrenergic Blockers TX

A

management of dysrhythmia from excessive SNS stimulation, a-fibrillation, & a-flutter (thought to slow the ventricular rate), post MI/CHF (thought to prevent v-fibrillation)

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124
Q

Nursing Concerns for BAB

A

use with Verapamil (Ca+ blocker) can increase RF HB and bradycardia and hypotension

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125
Q

Potassium

A

Main intracellular ion/involved with cardiac rhythm (contractility of the myocardium/heart muscle)

Normal value: 3.5-5.0 mEq/L

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126
Q

Hypokalemia

A

less than 3.5. Sx: ventricular dysrhythmias, muscle weakness, decreased DTRs, weak peripheral pulses

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127
Q

TX for more K

A

Increase dietary K+ rich foods

Oral (preferred): no more than 20 mEq/L/hr. Give with meals/assess swallowing. Pills can be scored.
20 mEq po every two hours because it can only be absorbed 20/hour

Peripheral IV: 20-40 mEq/L; do not exceed 20 mEq/hr: if burning occurs, stop and assess the site (mix this in a liquid!)

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128
Q

Hyperkalemia

A

greater than 5.0 mEq/L. Sx: dysrhythmias, V-fib, HB, cardiac arrest, muscle twitching, numbness in hands, feet, and mouth

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129
Q

TX of Hyperkalemia

A

Restrict dietary K+ rich foods

Sodium polystyrene (Kayexalate): binds K+ and causes diarrhea

IV administration of insulin/dextrose shifts K+ back into cells and lowers the serum potassium

Common with end stage renal failure

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130
Q

Potassium Channel Blockers

A

inhibits adrenergic stimulation:
Block potassium channels=prolongs duration of action potential=slow repolarization=prolong refractory period

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131
Q

Potassium Channel Blockers TX

A

IV for life threatening tachy-dysrhythmias (not first line r/t RF pulmonary toxicity)
PO for recurrent tachycardia, V & A fibrillation and A-Flutter

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132
Q

Potassium Channel Blockers SE

A

Bradycardia, hypotension, worsen or new dysrhythmia, pulmonary toxicity (pleuritic pain, lung sounds fever, change in respiratory pattern). Don’t like to use it for respiratory pts. (IV), hepatotoxicity (drinker), blurred vision/photosensitivity
ALT/AST: Liver function tests to check before administering this medication

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133
Q

K+ Channel Blockers Medications

A

amiodarone (IV in emergencies or PO), dofetilide (Tikosyn given IV over night for people. Risk of QT wave prolongation which shows us that the ventricles are not contracting at a fast enough rate for the system to sustain) ibutilide, sotalol

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134
Q

Calcium Channel Blockers Function

A

Block calcium ion channels=reduce automaticity in SA node and slow the conduction through AV node=slow HR=prolong refractory period.

**Avoid Grapefruit Juice

135
Q

Calcium Channel Blockers TX

A

supraventricular dysrhythmias (A-fib, SVT, atrial flutter) (@SA&AV nodes) tachycardia

*Can be an emergency medication for A-fib, SVT requiring IV administration

136
Q

Calcium Channel Blockers SE

A

Bradycardia, hypotension, (HA, dizziness, lightheadedness), flushed skin, MI, hepatotoxicity, PERIPHERAL EDEMA
***Caution with HB, sick sinus, HF, hypotension, Hepatic/renal insufficiency, pregnancy

137
Q

diltiazem, verapamil

A

Ca+ Channel Blocker Medications

138
Q

Adenosine

A

Used for SVT when a vagal maneuver does not work

Given as a rapid bolus because the high metabolism
Depresses the conduction @ AV node=restore NSR in SVT patients
Naturally occurring component of all body cells

139
Q

vagal maneuver

A

action to take when you need to stop an abnormally fast heart rate. Tell the patient to hold their breath and bear down for 20 seconds. Sticking your face in a bowl of icewater might work too.

140
Q

Atherosclerosis

A

sometimes called hardening or clogging of the arteries, is a buildup of cholesterol and fatty deposits called plaques on the inner walls of the arteries

141
Q

Coronary Heart Disease

A

Is the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis.
Chronic Coronary Artery Disease leads up to it

142
Q

Angina

A

Clinical Manifestation of Myocardial Ischemia

143
Q

Stable Angina

A

classic, typical, exertional angina (Stable will go away after like 5 minutes)

Results when myocardial O2 demand is greater than the O2 supply to the heart muscle

Often results from exercise, physical activity, elemental exposure to cold, emotions/stress

144
Q

TX for Stable Angina

A

thrombolytics (Lyce the clot) and interventional therapies (stents)

145
Q

Variant Angina

A

occurs at rest/minimal exertion, HS (at bedtime), same time of day, cyclic 3-6 mos, subsides

146
Q

Acute Coronary Syndrome (ACS)

A

Unstable Angina: ie: crescendo, rest or preinfarction angina
Acute pain occurs @ rest and lasts longer than 20 minutes
** can occur hours/days prior to acute myocardial infarction
** ACTION=IMperative! Time=Tissue

147
Q

2 Types of Myocardial Infarctions:

A

NSTEMI, STEMI

148
Q

NSTEMI

A

non-ST elevate Myocardial infarction. Interval between depolarization and polarization is there and not very much changed

149
Q

STEMI

A

greater than 20 minutes persistent ST elevation on EKG (Very dangerous)

150
Q

Cardiac Isoenzyme

A

Indicates damage to skeletal, visceral, or cardiac muscle. We would conclude cardiac

151
Q

Cardiac Troponin 1 and Troponin T

A

biomarker of myocyte injury

152
Q

Non-Pharmacologic Management of CAD

A

Cardiac Cath, coronary artery bypass graft (find a venule/artery that they cannot reopen so they cut out that artery that is bad and reconnect it to another artery), intracoronary stent

153
Q

Nitrates

A

Potent Vasodilators
Relax and dilate veins, arteries, and capillaries; increase blood flow; lower systolic pressure
Relief of and prevention of angina pain
Decreases preload and afterload

154
Q

Nitroglycerin Isosorbide dinitrate + Isosorbide mononitrate

A

Nitrates Examples

155
Q

Nitrates SE

A

Severe headache, dizziness, bradycardia, syncope, hypotension RT: hemodynamic changes responsible for preload reduction and vasodilation

156
Q

Nitrates Administration

A

Typically taken sublingual to prevent first pass effect in three doses: take one, 5 min, if pain stays, take 2 and wait 5 min, and make sure that you are going to the phone to call 911 if you need a third dose
Needs to be a brown bottle because it is degridated/light sensitive
Can be PO or translingual spray, or IV, or as a patch
Half life, 1-4 minutes. Rapidly absorbed

157
Q

Beta Adrenergic Blockers + CAD

A

decrease cardiac workload by slowing the heart rate which decreases blood pressure and reduces contractility which INCREASES the O2 to the heart.
Cornerstone daily medication for patients with angina.

158
Q

Calcium Channel Blockers + CAD

A

inhibits the influx of calcium entering through the slow channels which produces vasodilation of the peripheral blood vessels and coronary arteries. It does not affect the HR. Used for bradycardia. First pass metabolism is in the liver and it is fecal and urinary excretion

159
Q

Nifedipine

A

Dose related, Ca+ channel blocker, Grapefruit juice will increase the effect, this medication will increases serum digoxin levels, cannot be used with adrenergic stimulants

160
Q

Ranolazine

A

anti-ischemic metabolic modulator=first line treatment for chronic angina

161
Q

atorvastatin, cholestyramine, and niacin

A

Dyslipidemic drugs: management of patients with major risk factors for atherosclerosis and vascular disorders (CAD, stroke, and peripheral arterial insufficiency) when lifestyle changes alone do not reduce blood lipids

162
Q

Aspirin

A

antiplatelet effect with at lower doses effectively suppress platelet aggregation w/o without affecting important endothelial cell function. 81mg of Aspirin. Aspirin is the standard

163
Q

Glycoprotein (GP)

A

IIb/IIIa receptor antagonists inhibit platelet aggregation for post MI

164
Q

Post MI antiplatlets

A

The purpose of giving thrombolytic agents following a STEMI is to dissolve thrombi and reestablish blood flow as quickly as possible, prevent or limit tissue damage, and maximize functional improvement. The antiplatelets are daily medication for prevention.

165
Q

Adenosine diphosphate (ADP)

A

receptor antagonists have antiplatelet effects similar to aspirin.

166
Q

Morphine

A

opioid analgesic: pain/anxiety decrease preload. Primary reliever of pain management in post MI in patients with unacceptable levels of pain

167
Q

hypotension

A

Systolic pressure less than 90. This means that there is decreased perfusion, decreased blood flow, and decreased oxygen to the tissues in order for the tissues to survive

168
Q

Chronotropic effect

A

Change in HR

169
Q

Dromotropic effect

A

causing a change in speed of electrical conduction in the heart

170
Q

Inotropic effect

A

causing a change in the myocardial contraction

171
Q

Normotrophic Effect

A

Having normal blood pressure

172
Q

Pressor

A

effect that increases blood pressure

173
Q

Shock

A

clinical condition initiated by compromised oxygen delivery, oxygen consumption, and/or oxygen utilization that leads to cellular death or tissue hypoxia

174
Q

Acute hypotension is a sign of

A

Shock. Circulatory failure=hypotension=decrease in tissue perfusion

175
Q

Hypovolemic Shock

A

when there is not enough circulating volume. Low blood volume. This can be the result of trauma, hemorrhage, burns, diabetic insipidus and diabetic ketoacidosis. Children can get this from vomiting and diarrhea

176
Q

Cardiogenic Shock

A

pumping problem with the heart that can occur from an MI, dysrhythmia, or an improper valve closure problem between ventricle and atrium

177
Q

Obstructive Shock

A

when there is a mass (tumor) or accumulation of fluid in an area or a blood clot. Causes heart to not pump

178
Q

Disruptive Shock

A

when there is a state of massive vasodilation. For some reason the vessels get really big.

179
Q

Anaphylactic Shock

A

Type of Disruptive Shock. major vasodilation from a histamine release in a severe allergic reaction

180
Q

Neurogenic Shock

A

Type of Disruptive Shock when there is major vasodilation from high level spinal cord injury because there is a loss of signals for the sympathetic system. Message not sent to constrict

181
Q

Septic Shock

A

Type of Disruptive Shock major dilation release of inflammatory mediators as a result of an overwhelming infection. Tx: IV fluids and antibiotics

182
Q

Three stages of Shock

A

Compensative Phase
Uncompensated/Decompensated
Final “End Stage” Phase

183
Q

Compensative Phase of Shock

A

Preshock. When the body starts to sense that there is a low fluid volume it attempts to restore itself and return to homeostasis. When the heart senses that the blood volume is low it is gonna try to beat faster so that the body gets the blood that it needs. Can also compensate through vasoconstriction (SNS)

184
Q

Uncompensated/Decompensated Phase of Shock

A

r/t the compensation is not able to do the job and the shock is left untreated or undiagnosed. Typically because there is not enough blood to work with. This leads to organ dysfunction. WE are gonna see cardiac output, hypoperfusion, endothelial damage, microvascular thrombosis. Decreased capillary blood flow. WE heart rate will decrease. Patients will be clammy, cool, sweaty, restless, and decrease in urine output. Metabolic acidosis.

185
Q

Final “End Stage” Phase of Shock

A

Irreversible: Permanent tissue or organ damage. They are having multiple organ failure. Renal failure is the first to go. No urine production whatsoever. The patient is in lactic acidosis (buildup of acid causes an imbalance in pH. Not enough oxygen to break down glucose and glycogen)

186
Q

Therapy for Hypotension/Shock:

A

Adrenergic Agonist: Vasopressors
Epinephrine (Adrenaline)
Dopamine: Potent alpha adrenergic agonist
Dobutamine

187
Q

Adrenergic Agonist

A

cause potent peripheral arterial vasoconstriction, which will cause an increase in blood pressure and at times will also increase the heart rate, it will also increase the force of contraction and cardiac output

188
Q

Adrenergic Agonist Contraindications

A

cardiac dysrhythmias, angina pectoris, hypertension, hyperthyroidism, and cerebrovascular disease, narrow angle glaucoma. Toxic to the tissues. This medication has to be administered in a central line so that the medication goes right into the bloodstream

189
Q

Norepi, phenylephrine, epinephrine, dopamine

A

Adrenergic Agonists

190
Q

Epinephrine (Adrenaline)

A

stimulates beta and alpha adrenergic receptors: potent vasoconstrictor. Emergency medication that increases HR and constriction

191
Q

Dopamine

A

Potent alpha adrenergic agonist
Low dose: renal and coronary arteries
High dose: increase heart rate and vasoconstrictor (for shock)

192
Q

Dobutamine

A

Stimulates Beta 1 receptors
Low dose: increase contractility and increase cardiac output
Does not cause tachycardia
***incompatible with BICARB which is typically utilized as a buffer when we have lactic acidosis

193
Q

Phentolamine

A

alpha blocker that you use when leaking alpha adrenergic medication causes necrosis.

194
Q

Cardiomyopathy

A

disorder of the heart muscle where it becomes weak

195
Q

CHF

A

Complex clinical condition where the heart cannot pump enough blood to meet bodies O2 and nutritional needs

196
Q

Goal for CHF Patients

A

symptoms management. Decrease fluid management so that the heart can pump more efficiently

197
Q

Causes that impair pumping ability of the heart

A

hyperthyroidism (thermoregulator). Excessive fluids/blood transfusion. When blood is thicker it makes the heart work harder. Fluid volume overload. Antidysrhythmic medications. Water retention.

198
Q

Endothelial Dysfunction

A

narrowing of vessel lumen which increases pressure. Leads to clot formation. Leads to vasoconstriction

199
Q

Systolic Heart Failure

A

Failure of ventricle contraction. Most common. Reduced EF

200
Q

Diastolic Heart Failure

A

Failure of Filling: Stiff noncompliant muscle. Normal EF

201
Q

Right Sided Heart Failure sx

A

Weight gain, JVD, Peripheral Edema, Fatigue
Ascites (swelling around abdomen), Enlarged liver and spleen, Lack of appetite, Weight gain

202
Q

Core pulmonale

A

enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance.

203
Q

Left-Sided Heart Failure sx

A

Right ventricle is pumping really hard against narrow blood vessels. SOB
Crackles, Activity intolerance, Dizziness, Because the blood is backing up from the left side of the heart and it is staying in the lungs, Tacipnea: rapid breathing. Confused: Orthopnea

204
Q

Digoxin

A

Management of mild-moderate heart failure. Positive inotropic effect. Management of atrial fibrillation: negative chronotropic effect which SLOWs the heart. Allows more Ca+ to enter the cells which increases intracellular Ca+ which decreases the workload of the heart

205
Q

Digoxin Adverse Effects

A

weakness, HA, Drowsiness, vision changes, GI upset/anorexia, Arrhythmias, breast enlargements
Monitor for improving signs of HF/Afib and monitor for DIG TOXICITY. HOLD if serum level is greater than 2nm/mL

206
Q

Therapeutic Normal dig levels

A

0.8-2nm/mL

207
Q

Contraindications for Digoxin

A

PMHx of V tach/V fib, HB/Sick sinus, Acute MI, Renal insufficiency, Electrolyte abnormalitie

208
Q

Signs of digoxin toxicity:

A

Yellow/green vision blurring
Ventricular rhythm changes
Abdominal discomfort
Premature ventricular contractions

209
Q

Which blood results can cause dig toxicity even when the dig levels are WNL

A

hypokalemia, hypomagnesemia, and hypercalcemia

210
Q

digoxin antidote

A

digoxin immune Fab

211
Q

Phosphodiesterase Inhibitor

A

Long term bridge therapy (combines the heart) in heart failure, Increase Ca++ in cell.
Increase the force contraction in the ventricle, positive inotropic effect, relaxation in the vascular smooth muscle, systemic and pulmonary dilation, decrease in preload and afterload so the tired heart does not have to pump so hard against preload and afterload

212
Q

milrinone

A

Phosphodiesterase Inhibitor

213
Q

milrinone SE

A

Thrombocytopedia, burning at injection site, anorexia, N/V, cp

214
Q

Human B Type Naturinic Peptides

A

Hormones that help maintain sodium and fluid balance which reduces preload and afterload

215
Q

Human B Type Naturinic Peptides Action

A

release increases sodium excretion by the kidney and diuresis, direct vasodilation, increased glomerular filtration rate. Gonna help the kidneys to release the sodium. Not great for someone with kidney or renal disease

216
Q

Nestride

A

Human B Type Naturinic Peptides Action

217
Q

Adverse Effects of Nestride

A

hypotension, HA, N/V, backpain, dizziness, ventricular tachycardia, anxiety, insomnia, bradycardia
Monitor BP and urine output and BMP for sodium

218
Q

Sacubitril/valsartin

A

Management of chronic heart failure in patients with reduced ejection fraction

219
Q

Sacubitril/valsartin Therapeutic Action

A

Sacubitril inhibits the enzyme neprilysin, responsible for degradation of atrial and brain natriuretic peptide (BNP), the peptides responsible for lowering blood pressure and blood volume along with Valsartin (ARB)

220
Q

Contraindication Sacubitril/valsartin

A

Lithium, pregnancy, must be on birth control

221
Q

Sacubitril/valsartin AE

A

hypotension, hyperkalemia, cough, renal impairment, dizziness, angioedema may also occur

222
Q

Sinoatrial node modulators

A

Selective inhibition in the SA node=decreased firing from the SA node=decreased heart rate=allows more ventricular filling. Reduce risks in worsening heart failure for patients who have chronic heart failure while they are in the hospital

223
Q

Ivabradine

A

Sinoatrial node modulators

224
Q

Ivabradine SE

A

Bradycardia, hypotension, and fibrillation, and phosphine (a ring or spot of light caused by pressure on the eye orbital)

225
Q

Contraindications for Ivabradine

A

acute, decompensated heart failure, bradycardia, hypotension, heart blocks, sick sinus syndrome, pacemaker patients, severe hepatic impairment, grapefruit juice

226
Q

diarrhetic + Heart Failure

A

Pt. will almost always be on a diarrhetic.
If we see a 4lb increase in body weight we need to see them. Sodium and water stick to the body!
Diuretics nighttime dose is always at around 5pm
PO first, IV second,

227
Q

Spironolactone

A

K+ sparing diuretic

228
Q

lipoproteins

A

Each lipoprotein contains cholesterol, phospholipids, and triglyceride bound to protein

229
Q

cluster of conditions that occur together that end up increasing the risk of heart disease, stroke, and type II diabetes.

A

High waist circumference
High triglyceride levels resulting from high carbs and dietary proteins
High LDL (low density lipoprotein)
Low HDL (High density lipoprotein)
High blood pressure
High fasting glucose
hypertension

230
Q

Dyslipidemia

A

AKA hyperlipidemia: increase levels of lipids in the blood
Major risk factor for CAD
Associated with atherosclerosis

231
Q

s/sx associated with dyslipidemia

A

MI
Ischemia
CVA
Peripheral arterial occlusive disease

232
Q

Primary Dyslipidemia

A

genetic/familial
Mutation in the LDL receptor and they have an increase in their LDL lifelong
1/500 people

233
Q

Secondary Dyslipidemia

A

habit/lifestyle
Alcoholism, DM, hypothyroidism
Obesity. Obstructive liver disease

234
Q

HIgh cholesterol Symptoms

A

Loose stools
Poor appetite
Fatigue
Depression
Weight gain
Bumps around their eyes
Stomach distension
Heart pain
Aching pain

235
Q

National Cholesterol Education Program III Treatment Guidelines

A

Total Serum Cholesterol (less than 200)
LDL (less than 100)
HDL (between 40-60, and greater than 60 is good)
Treatment according to total and LDL cholesterol because these risk for cardiovascular disease

236
Q

Assessment and Treatment plan for HIgh cholesterol

A
  1. Determine hypoprotein level after 9-12 hour fast
  2. Identification of presence of atherosclerotic disease that confers high risk for coronary heart disease events
  3. Determine other risk factors besides a high LDL
237
Q

LDL

A

low density lipoprotein. BAD

238
Q

HDL

A

High density lipoprotein

239
Q

Characteristics of Antidyslipidemics

A

Decrease blood lipids
prevent /delay atherosclerosis plaque development
Promote regression of existing atherosclerotic plaque.
Reduce morbidity and mortality from cardiovascular disease

240
Q

hydroxymethylglutaryl-coenzyme A reductase inhibitors

A

Decrease cholesterol production=decreases total cholesterol, LDL, VLDL and triglycerides without reducing HDL

241
Q

Atorvastatin, pradistatin, Rosuvastatin, Simvastatin

A

hydroxymethylglutaryl-coenzyme A reductase inhibitors examples

242
Q

Pharmacokinetics of hydroxymethylglutaryl-coenzyme A reductase inhibitors

A

extensive first pass effect (liver)/food decreases absorption rate/80-85% excreted in stool, the rest excreted in the urine

243
Q

hydroxymethylglutaryl-coenzyme A reductase inhibitors Side Effects

A

MYALGIAS (dysfunction in the muscle fibers), leg pain, nuasa, constipation, diarrhea

244
Q

hydroxymethylglutaryl-coenzyme A reductase inhibitors
Drug Interactions

A

MG+ antacids, “azole” antifungals, some antibiotics, cholestyramine

245
Q

hydroxymethylglutaryl-coenzyme A reductase inhibitors Considerations

A

Evening or HS administration (2100) medication r/t cholesterol synthesis occurs at this time of day
Avoid grapefruit juice, vitamin B, pomegranate juice
Monitor liver function tests because it has a big first pass effect
Watch for rhabdomyolysis (severe muscle cramps, cola colored urine, extreme fatigue) stop med and call doctor.
BLACK BOX: X CATEGORY

246
Q

Bile Acid Sequestrants

A

Binds bile acids in the intestinal lumen = bile acids excreted via stool= prevents recirculation to liver = stimulates increase bile acid synthesis from cholesterol in liver = increases cholesterol to liver = lowers serum LDL

247
Q

Cholestyramine

A

Bile Acid Sequestrant example

248
Q

Cholestyramine Pharmacokinetics

A

not absorbed with oral administration. Excreted unchanged in stool/decrease LD within a week of use and max level will maximize in 1 month

249
Q

cholestyramine SE

A

GI fullness, flatulence, constipation, diarrhea

250
Q

Cholestyramine Considerations

A

It stops absorption of (DIG, glipizide, folic acid, propranolol, thyroid hormone, thiazide diuretics, warfarin)

251
Q

Fibrates

A

increase oxidation of fatty acids in the liver and muscle tissue. Decrease hepatic production of triglycerides, VLDL, and increase HDL

252
Q

Fenofibrate + gemfibrozil

A

Fibrates Examples

253
Q

Fibrates Pharmacokinetics

A

oral administration/highly protein bound, peak 6-8 hours, liver metabolism, urinary excretion

254
Q

Fenofibrate + gemfibrozil Side effects

A

RF gallstones: not for pts. With existing or preexisting gallbladder disease

255
Q

Nursing Concerns for Fenofibrate

A

can enhance the effects of warfarin, increase RF myopathies or rhabdomyolysis with STATINS

256
Q

gemfibrozil

A

must be taken on an empty stomach

257
Q

Cholesterol Absorption inhibitors

A

Inhibit absorption of cholesterol in the small intestines & decreases delivery of intestinal cholesterol to the liver = reduced hepatic cholesterol stores , increasing cholesterol clearance from the blood

258
Q

Ezetimibe

A

Cholesterol Absorption inhibitor

259
Q

Ezetimibe: Pharmacokineteics

A

protein bound, metabolized in small intestine and liver and excreted in stool. Peak effect after in4-12 hours.

260
Q

Ezetimibe Consideration

A

Category C

261
Q

PCSK9 Inhibitors

A

antibody that inactivates protein in the liver that regulates lifespan of cholesterol, promoting modulation of the receptors=prolong receptor activity=promoting clearance of cholesterol=can have a 60-70% reduction in LDL

262
Q

Alirocumab

A

PCSK9 Inhibitor

263
Q

Alirocumab Consideration

A

Used for patients with PRIMARY hyperlipidemia when their statin dose is maxed out

subQ every 2-4 weeks/doses vary. 3-7 day max serum concentrations

264
Q

Niacin (Vitamin B3)

A

boosts levels of healthy HDL levels and lowers triglycerides and modestly lowers LDL

265
Q

Niacin (Vitamin B3) SE

A

facial flushing, stomach upset, diarrhea, can raise blood sugar (not good for DM)

266
Q

Omega 3 Fatty Acids

A

Dyslipidemic

267
Q

Advicor

A

extended release niacin and lovestatin combination medication

268
Q

Simcor

A

simvastatin and niacin combination therapy

269
Q

Hematopoietic Disorder

A

diseases that cause the blood to change. Not enough, too much, RBC cells too large, viscosity of the blood, hemoglobin levels

270
Q

Hematopoiesis

A

the process of making blood that happens in the bone marrow

271
Q

stem cells

A

grow into all three types of blood cells (red, white, platelets). They make copies of themselves and produce mature blood cells and then leave the blood marrow.

272
Q

Hematopoietic Growth Factor

A

determines survival and proliferation of hematopoietic lineage and can transduce a genuine lineage determining signal in hematopoiesis and initiate the cell maturation process

273
Q

Hematopoietic Cytokines

A

Extracellular ligands that stimulate hematopoietic cells to differentiate into eight principle types of blood cells (white blood cells)
Regulate many cellular activities
Act as chemical messengers among cells
Act as growth factors for blood cells
Perform by binding to receptor on target cells

274
Q

Interleukins

A

Affect immunogenic cell response. They are either Stimulator or Suppressive

275
Q

Erythropoietin

A

Hormone secreted by kidneys which stimulates RBC differentiation, Maturation, and proliferation. Stimulates bone marrow to produce RBC (transport vehicles)

Conditions that will trigger this are hemorrhage, anemia, COPD, and high altitude
Higher red blood cells means higher ability for blood to carry oxygen to the cells

276
Q

Immune System

A

Immune system cells identify and remove injured, damaged, dead or malignant cells.

277
Q

Leukocytes

A

(fighters) that circulate in blood and lymphatic vessels or reside in lymphoid tissues. Make up

278
Q

CBC w/ Differential

A

gives a count of each type of white blood cells. Helps a doctor know exactly WHY a WBC is up

279
Q

Leukocytosis

A

increase in WBC

280
Q

Leukopenia

A

Decrease in WBC

281
Q

Anemia

A

a lack of RBC or disfunctional RBC in the body which leads to reduction of Oxygen flow to body’s organ because the RBC houses hemoglobin which carry the oxygen to the tissue.

282
Q

Iron Anemia

A

decrease of Iron in the blood which leads to a decrease in RBC count. Can be because of store depletions.

At Risk: Menstruating women, lactating women, rapidly growing kids, losing blood at large volume through a GI bleed

283
Q

Pernicious Anemia

A

deficiency of Vitamin B12: tx: IMb12 injections or B12 oral supplements

284
Q

Megaloblastic Anemia

A

a person has larger than normal blood cells due to inhibition of DNA synthesis during RBC production. Cell cycle cannot migrate from G2 to the mitosis phase so the cells get bigger and bigger without division

285
Q

Megaloblastic Anemia S/Sx

A

glossy red tongue and diarrhea.
Results from a deficiency of Vitamin B12 and folate.

286
Q

Sickle Cell Anemia

A

Sickle cells do not allow the O2 to attach which limits perfusion.

287
Q

Hydroxyurea/antimetabolite:

A

helps prevent formation of “sickle” shaped cells

288
Q

Immunostimulants

A

drugs that stimulate/enhance the immune system by inducing activation of increasing any of its components

Used to restore normal function or increase the ability of the immune system to eliminate harmful invaders

Typically these are injected

289
Q

Epoetin alpha
darbepoetin

A

Induces Erythropoiesis leading to an increase in Hgl and Hct levels

Treatment of anemia in renal failure, AIDS, and cancer

Stimulates the patient’s own body to avoid blood transfusion.

290
Q

Epoetin alpha/darbepoetin Administration

A

IV/SQ. Metabolized in serum/excreted in urine. injectable with an airlock. Monitor CBC for INCREASE in RBC, Hgb, Hct, increase energy and exercise tolerance

291
Q

Epoetin alpha/darbepoetin Considerations

A

uncontrolled hypertension (we don’t wanna make the blood even thicker!)/allergy/normal renal function (kidneys are producing enough on its own)

292
Q

Granulocyte Colony Stimulating Factors

A

Stimulate blood cell production in bone marrow for patients with neutropenia (chemotherapy induced febrile neutropenia, acute myeloid leukemia, cancer patients receiving bone marrow transplants, or chronic idiopathic neutropenia)

293
Q

Filgrastim

A

stimulates neutrophil progenitor cell proliferation and differentiation in bone marrow=increase number of mature neutrophils

294
Q

Filgrastim Considerations

A

SQ/IV. Completely absorbed over four days

flu like symptoms, fatigue, bone pain, thrombocytopenia (bleeding gums/ease of bruising)

295
Q

Ferrous aspartate
Ferrous gluconate
ferrous sulfate
iron dextran

A

regain positive iron balance, treatment of iron deficient anemia

IV, PO
Z-track for IM-iron dextran
Iron is Absorbed in small intestine

296
Q

ferrous sulfate Adverse Effects

A

GI effects: constipation
Administer between meals if possible (increase absorption)
Vitamin C given with iron can increase absorption
If oral liquid, use straw because it stains the teeth

297
Q

Plasminogen and Fibrin

A

used to form the clot which stops the blood flow and keeps the blood vessel repaired.

298
Q

Plasmin

A

dissolves the clot once it is all healed

299
Q

Liver

A

primary organ responsible for clotting factors

300
Q

Intrinsic Pathway

A

trauma INSIDE the blood vessel itself. OR blood is exposed to collagen factor 12

301
Q

Extrinsic Pathway

A

vascular tissue trauma

302
Q

Thrombogenesis

A

Formation and dissolving of thrombi
Normal Body Defense

303
Q

Arterial Thrombosis

A

obstruct arterial blood flow

304
Q

Venous Thrombosis

A

result of venous stasis
Less cohesive than arterial thrombus and travel quickly and detach more easily
MORE severe than arterial thrombosis

305
Q

Prophylactic DVT prevention

A

Heparin subque

306
Q

Atherosclerosis

A

Elevated serum lipid levels
Lipid Filled macrophages
Fibrous Plaques and lesions
Severe ulceration and scarring tissue

307
Q

Antithrombotic + Antithrombolitic

A

Anticoagulants
Antiplatelets (platelet life: 7-10 days)
Thrombolytics

308
Q

Anticoagulants

A

DO NOT dissolve formed clots

Prevent formation of new clots
management of thromboembolic disorders

309
Q

Thrombophlebitis

A

vein inflammation usually occurs by irritation to a venus venule by a clot

310
Q

Heparin

A

Given to prevent new clot formation and extension of clots present

IV: monitor aPTT/PTT

311
Q

Test and normal range for heparin

A

aPTT/PTT: 60-80
SQ: prophylaxis for DVT formation prevention in bed restricted hospital patients (dose 5000u/mL)

312
Q

Heparin Antidote

A

protamine sulfate (basic)

313
Q

Warfarin Test and Result

A

PT/INR: 2-3

314
Q

Antidote for Warfarin

A

Vitamin K+

315
Q

Considerations for Warfarin

A

avoid foods high in vitamin K
Avoid grapefruit juice, cranberry juice, and alcohol (enhance the effect)
Kale, broccoli, soybean oils

316
Q

Fondaparinux

A

Factor Xa Inhibitor
SQ injection only
Extremely expensive ($3726/10 doses)
Prefilled

317
Q

Dabigatran

A

Direct thrombin inhibitor
Tx: afib and stroke prevention
PO bid

318
Q

Dabigatran Antidote

A

Idarucizumab

319
Q

Rivaroxaban

A

Factor Xa Inhibitor
Tx of afib, stroke prevention, secondary DVT (DVT came from a known cause) prevention
PO once a day

320
Q

Apixaban

A

Factor Xa inhibitor
Tx of afib, stroke prevention,
Given bid

321
Q

BLACK BOX for Xa Inhibitors

A

don’t stop abruptly due to rebound thrombotic event

322
Q

Ecchymosis

A

Excessive bruising

323
Q

Subdural hematoma

A

Bleed in the brain

324
Q

Hemoptisis

A

Bloody sputum

325
Q

Antiplatelets

A

Inhibit platelet activation
Inhibit platelet adhesion
Inhibit platelet aggregation
Inhibit procoagulant acuity

326
Q

Clopidogrel

A

Antiplatelet
Irreversibly inhibit ADP receptors on the surface of platelets. No antidote
Extensive first pass effect. Onset of action is slow so a loading dose is necessary
Can be used in conjunction with aspirin
Significant individual variability in response
Most common SE=pruritus (itching), rash, purpura, diarrhea

327
Q

Thromboxane A2 Inhibitors

A

Antiplatelet
Inhibits the synthesis of prostaglandins=prevents formation of thromboxane A2=prevents platelet aggregation

328
Q

81mg Aspirin

A

Thromboxane A2 Inhibitor

329
Q

Abciximab

A

monoclonal antibodies that prevent the binding of fibrinogen, this action will inhibit platelet aggregation.
Used for interventional procedures with ASA and Heparin

330
Q

Cilostazol

A

inhibits platelet aggregation and produces vasodilation
Used for intermittent claudication

331
Q

Anagrelide

A

inhibit platelet aggregation induced by cAMP phosphodiesterase
Reduce platelet counts R/T essential thrombocythemia

332
Q

intermittent claudication

A

Pain with activity caused by reduced blood flow to a limb. Symptom of PVD

333
Q

Thrombolytic Agents

A

given to dissolve thrombi and stimulate conversion of plasminogen to plasmin (breaks down thrombin)

334
Q

Alteplase

A

High Risk Emergency medication that thins blood and gets out of the blood in 10 minutes. This is used for stroke or blood clots
Headache and hypotension indicate that the patient is bleeding internally and this is BAD when taking this medication.

Nursing (17 decks)

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